ArticlePloS one2014
Experimental myocardial infarction induces altered regulatory T cell hemostasis, and adoptive transfer attenuates subsequent remodeling.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 76 citations in OpenAlex.
- Regulatory T cells and peripheral immune tolerance: key mechanisms and therapeutic strategies for cardiovascular diseases.Frontiers in immunology · 2026Review
- Stem cell-derived extracellular vesicles as immunomodulators: a novel paradigm for post-myocardial infarction repair and regeneration.Frontiers in pharmacology · 2026Review
- Plasma Small Extracellular Vesicles of Ischemic Cardiomyopathy Aggravate Ventricular Remodeling Post-Myocardial Infarction and Promote miR-223-3p-mediated Dysfunction in Regulatory T Cells.Journal of cardiovascular translational research · 2025Article
- sRAGE inhibits myocardial ischemia/reperfusion injuries via regulating Treg cells.Cell & bioscience · 2025Article
- Regulatory T cells: a promising new therapeutic target in ventricular remodeling after myocardial infarction.Frontiers in immunology · 2025Review
- Identification and validation of differentially expressed disulfidptosis-related genes in hypertrophic cardiomyopathy.Molecular medicine (Cambridge, Mass.) · 2024Article
- Local administration of regulatory T cells promotes tissue healing.Nature communications · 2024Article
- IL-4-Induced Gene 1: A Potential Player in Myocardial Infarction.Reviews in cardiovascular medicine · 2024Review
- Tregs delivered post-myocardial infarction adopt an injury-specific phenotype promoting cardiac repair via macrophages in mice.Nature communications · 2024Article
- Treg-tissue cell interactions in repair and regeneration.The Journal of experimental medicine · 2024Review
- Role of Treg cell subsets in cardiovascular disease pathogenesis and potential therapeutic targets.Frontiers in immunology · 2024Review
- [Cardiac progenitor cells-derived exosomes alleviate myocardial injury by regulating Treg cell differentiation through the mTOR pathway in mice with myocardial infarction].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Xin-Li formula attenuates heart failure induced by a combination of hyperlipidemia and myocardial infarction in rats via Treg immunomodulation and NLRP3 inflammasome inhibition.Journal of traditional and complementary medicine · 2023Article
- Recruitment of myeloid‑derived suppressor cells and regulatory T‑cells is associated with the occurrence of acute myocardial infarction.Biomedical reports · 2023Article
- Control of the post-infarct immune microenvironment through biotherapeutic and biomaterial-based approaches.Drug delivery and translational research · 2023Review
- The Role of Regulatory T Cells in Heart Repair After Myocardial Infarction.Journal of cardiovascular translational research · 2023Review
- Single-cell RNA sequencing to identify cellular heterogeneity and targets in cardiovascular diseases: from bench to bedside.Basic research in cardiology · 2023Review
- Kynurenic acid, a key L-tryptophan-derived metabolite, protects the heart from an ischemic damage.PloS one · 2023Article
- Targeting regulatory T cells for cardiovascular diseases.Frontiers in immunology · 2023Review
- CD69 expression on regulatory T cells protects from immune damage after myocardial infarction.The Journal of clinical investigation · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIschemic cardiac damage is associated with upregulation of cardiac pro-inflammatory cytokines, as well as invasion of lymphocytes into the heart. Regulatory T cells (Tregs) are known to exert a suppressive effect on several immune cell types. We sought to determine whether the Treg pool is influenced by myocardial damage and whether Tregs transfer and deletion affect cardiac remodeling. METHODS AND
resultsThe number and functional suppressive activity of Tregs were assayed in mice subjected to experimental myocardial infarction. The numbers of splenocyte-derived Tregs in the ischemic mice were significantly higher after the injury than in the controls, and their suppressive properties were significantly compromised. Compared with PBS, adoptive Treg transfer to mice with experimental infarction reduced infarct size and improved LV remodeling and functional performance by echocardiography. Treg deletion with blocking anti-CD25 antibodies did not influence infarct size or echocardiographic features of cardiac remodeling.
conclusionTreg numbers are increased whereas their function is compromised in mice with that underwent experimental infarction. Transfer of exogeneous Tregs results in attenuation of myocardial remodeling whereas their ablation has no effect. Thus, Tregs may serve as interesting potential interventional targets for attenuating left ventricular remodeling.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.